The regulation of aging: does autophagy underlie longevity?

被引:132
作者
Vellai, Tibor [1 ]
Takaks-Vellai, Krisztina [1 ]
Sass, Miklos [2 ]
Klionsky, Daniel J. [3 ,4 ,5 ]
机构
[1] Eotvos Lorand Univ, Dept Genet Cell & Dev Biol, H-1117 Budapest, Hungary
[2] Eotvos Lorand Univ, Dept Anat Cell & Dev Biol, H-1117 Budapest, Hungary
[3] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA
[4] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Dept Biol Chem, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
EXTENDS LIFE-SPAN; AGE-RELATED DECLINE; CAENORHABDITIS-ELEGANS; PROTEIN-DEGRADATION; CALORIC RESTRICTION; DIETARY RESTRICTION; OXIDATIVE STRESS; GENES; KINASE; TOR;
D O I
10.1016/j.tcb.2009.07.007
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
The accumulation of cellular damage is a feature common to all aging cells and leads to decreased ability of the organism to survive. The overall rate at which damage accumulates is influenced by conserved metabolic factors (longevity pathways and regulatory proteins) that control lifespan through adjusting mechanisms for maintenance and repair. Autophagy, the major catabolic process of eukaryotic cells that degrades and recycles damaged macromolecules and organelles, is implicated in aging and in the incidence of diverse age-related pathologies. Recent evidence has revealed that autophagic activity is required for lifespan extension in various long-lived mutant organisms, and that numerous autophagy-related genes or proteins are directly regulated by longevity pathways. These findings support the emerging view that autophagy is a central regulatory mechanism for aging in diverse eukaryotic species.
引用
收藏
页码:487 / 494
页数:8
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